title: [Effects of early statin treatment on inflammatory biomarkers and clinical deterioration in patients with acute ischemic stroke].
abstract: We prospectively studied the effects of early statin treatment on stroke-induced changes in the levels of inflammatory biomarkers. Patients admitted within 48 hours after the onset of ischemic stroke were enrolled. They were divided into 2 groups according to their lipid profiles and history of statin treatment. In patients who had received statin treatment prior to admission and those who had abnormal lipid profiles on admission, daily treatment with 10 mg atorvastatin was initiated within 48 hours after the onset of stroke (Statin group; n = 45). In patients who had normal lipid profiles on admission, statin was not administered for at least 2 weeks after admission (Non-Statin group; n = 101). The serum concentrations of interleukin (IL)-6, IL-10, IL-18, matrix metalloproteinase (MMP)-2, MMP-9, and high sensitive C-reactive protein were measured on days 1, 3, 7, and 14. In percentage changes in serially measured circulating IL-6 levels, a significant interaction between group and repeated measures (group X time factor) was demonstrated (p = 0.047). Frequency of neurological deterioration episodes (NIHSS score > or = 2) during 14 days after admission was lower in the Statin group than in the Non-Statin group, however the difference did not reach statistically significant level (7.9% vs 20.2%, p = 0.118). The initiation of usual dose of atorvastatin early after the onset of ischemic stroke significantly decreased the elevation of IL-6 and may protect against the early neurological deterioration. Circulating levels of IL-6 may be one of the candidates for monitoring the acute effects of statin. Further studies wherein IL-6 levels are monitored in larger samples would be feasible for investigating the effect of early treatment with usual dose of atorvastatin on the functional outcome.
authors.affiliation: Department of Neurology, St. Marianna University School of Medicine.
authors.forename: Kenzo
authors.initials: K
authors.lastname: Sakurai
authors.forename: Kenji
authors.initials: K
authors.lastname: Isahaya
authors.forename: Satoshi
authors.initials: S
authors.lastname: Takaishi
authors.forename: Bunta
authors.initials: B
authors.lastname: Kato
authors.forename: Kanako
authors.initials: K
authors.lastname: Shimizu
authors.forename: Kana
authors.initials: K
authors.lastname: Shimomura
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Tokuyama
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Hasegawa
mesh_terms: D000368:Aged; D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood*; D002097:C-Reactive Protein / Q000032:analysis; D002544:Cerebral Infarction / Q000188:drug therapy* / Q000503:physiopathology; D005260:Female; D006538:Heptanoic Acids / Q000008:administration & dosage; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D007378:Interleukins / Q000097:blood; D008297:Male; D020782:Matrix Metalloproteinases / Q000097:blood; D011446:Prospective Studies; D011758:Pyrroles / Q000008:administration & dosage; D013997:Time Factors
chemical_list: D015415:Biomarkers; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007378:Interleukins; D011758:Pyrroles; D002097:C-Reactive Protein; D000069059:Atorvastatin; D020782:Matrix Metalloproteinases